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Neuroimaging studies have demonstrated gray matter (GM) volume abnormalities in substance users. While the majority of substance users are polysubstance users, very little is known about the relation between GM volume abnormalities and polysubstance use.In this study we assessed the relation between GM volume, and the use of alcohol, tobacco, cocaine and cannabis as well as the total number of substances used, in a sample of 169 males: 15 non-substance users, 89 moderate drinkers, 27 moderate drinkers who also smoke tobacco, 13 moderate drinkers who also smoke tobacco and use cocaine, 10 heavy drinkers who smoke tobacco and use cocaine and 15 heavy drinkers who smoke tobacco, cannabis and use cocaine.Regression analyses showed that there was a negative relation between the number of substances used and volume of the dorsal medial prefrontal cortex (mPFC) and the ventral mPFC. Without controlling for the use of other substances, the volume of the dorsal mPFC was negatively associated with the use of alcohol, tobacco, and cocaine. After controlling for the use of other substances, a negative relation was found between tobacco and cocaine and volume of the thalami and ventrolateral PFC, respectively.These findings indicate that mPFC alterations may not be substance-specific, but rather related to the number of substances used, whereas, thalamic and ventrolateral PFC pathology is specifically associated with tobacco and cocaine use, respectively. These findings are important, as the differential alterations in GM volume may underlie different cognitive deficits associated with substance use disorders.

Holding a handrail or using a cane may decrease the energy cost of walking in stroke survivors. However, the factors underlying this decrease have not yet been previously identified. The purpose of the current study was to fill this void by investigating the effect of physical support (through handrail hold) and/or somatosensory input (through light touch contact with a handrail) on energy cost and accompanying changes in both step parameters and neuromuscular activity. Elucidating these aspects may provide useful insights into gait recovery post stroke.Fifteen stroke survivors participated in this study. Participants walked on a treadmill under three conditions: no handrail contact, light touch of the handrail, and firm handrail hold. During the trials we recorded oxygen consumption, center of pressure profiles, and bilateral activation of eight lower limb muscles. Effects of the three conditions on energy cost, step parameters and neuromuscular activation were compared statistically using conventional ANOVAs with repeated measures. In order to examine to which extent energy cost and step parameters/muscle activity are associated, we further employed a partial least squares regression analysis.Handrail hold resulted in a significant reduction in energy cost, whereas light touch contact did not. With handrail hold subjects took longer steps with smaller step width and improved step length symmetry, whereas light touch contact only resulted in a small but significant decrease in step width. The EMG analysis indicated a global drop in muscle activity, accompanied by an increased constancy in the timing of this activity, and a decreased co-activation with handrail hold, but not with light touch. The regression analysis revealed that increased stride time and length, improved step length symmetry, and decreased muscle activity were closely associated with the decreased energy cost during handrail hold.Handrail hold, but not light touch, altered step parameters and was accompanied by a global reduction in muscle activity, with improved timing constancy. This suggests that the use of a handrail allows for a more economic step pattern that requires less muscular activation without resulting in substantial neuromuscular re-organization. Handrail use may thus have beneficial effects on gait economy after stroke, which cannot be accomplished through enhanced somatosensory input alone.

A large evidence-based review on the effects of a moderate consumption of beer on human health has been conducted by an international panel of experts who reached a full consensus on the present document. Low-moderate (up to 1 drink per day in women, up to 2 in men), non-bingeing beer consumption, reduces the risk of cardiovascular disease. This effect is similar to that of wine, at comparable alcohol amounts. Epidemiological studies suggest that moderate consumption of either beer or wine may confer greater cardiovascular protection than spirits. Although specific data on beer are not conclusive, observational studies seem to indicate that low-moderate alcohol consumption is associated with a reduced risk of developing neurodegenerative disease. There is no evidence that beer drinking is different from other types of alcoholic beverages in respect to risk for some cancers. Evidence consistently suggests a J-shaped relationship between alcohol consumption (including beer) and all-cause mortality, with lower risk for moderate alcohol consumers than for abstainers or heavy drinkers. Unless they are at high risk for alcohol-related cancers or alcohol dependency, there is no reason to discourage healthy adults who are already regular light-moderate beer consumers from continuing. Consumption of beer, at any dosage, is not recommended for children, adolescents, pregnant women, individuals at risk to develop alcoholism, those with cardiomyopathy, cardiac arrhythmias, depression, liver and pancreatic diseases, or anyone engaged in actions that require concentration, skill or coordination. In conclusion, although heavy and excessive beer consumption exerts deleterious effects on the human body, with increased disease risks on many organs and is associated to significant social problems such as addiction, accidents, violence and crime, data reported in this document show evidence for no harm of moderate beer consumption for major chronic conditions and some benefit against cardiovascular disease.

ObjectiveTo characterize neurophysiological subcortical abnormalities in myoclonus–dystonia and their modulation by alcohol administration.MethodsCerebellar associative learning and basal ganglia–brainstem interaction were investigated in 17 myoclonus–dystonia patients with epsilon‐sarcoglycan (SGCE) gene mutation and 21 age‐ and sex‐matched healthy controls by means of classical eyeblink conditioning and blink reflex recovery cycle before and after alcohol intake resulting in a breath alcohol concentration of 0.08% (0.8g/l). The alcohol responsiveness of clinical symptoms was evaluated by 3 blinded raters with a standardized video protocol and clinical rating scales including the Unified Myoclonus Rating Scale and the Burke–Fahn–Marsden Dystonia Rating Scale.ResultsPatients showed a significantly reduced number of conditioned eyeblink responses before alcohol administration compared to controls. Whereas the conditioning response rate decreased under alcohol intake in controls, it increased in patients (analysis of variance: alcohol state × group, p = 0.004). Blink reflex recovery cycle before and after alcohol intake did not differ between groups. Myoclonus improved significantly after alcohol intake (p = 0.016). The severity of action myoclonus at baseline correlated negatively with the conditioning response in classical eyeblink conditioning in patients.InterpretationThe combination of findings of reduced baseline acquisition of conditioned eyeblink responses and normal blink reflex recovery cycle in patients who improved significantly with alcohol intake suggests a crucial role of cerebellar networks in the generation of symptoms in these patients. Ann Neurol 2017;82:543–553

Repeated treatment of rats with ethanol (1 g/kg, once daily for 15 days) enhanced the locomotor effect of morphine, 3 weeks post-treatment. This ethanol-induced long-term behavioural sensitization to morphine was associated with an increase in the electrically evoked release of [3H]dopamine (DA) and [14C]acetylcholine (ACh) from nucleus accumbens slices. A similar enhanced responsiveness of accumbal dopaminergic and cholinergic neurons to depolarization was apparent 3 weeks after repeated morphine, amphetamine or cocaine administration. Prior ethanol exposure also caused a long-term enhancement of electrically evoked release of [3H]DA and [14C]ACh from slices of the caudate-putamen. Unlike the locomotor effect of morphine, that of amphetamine was not enhanced in ethanol-pretreated rats. These data indicate that ethanol administration may cause long-term behavioural sensitization associated with adaptive changes in dopaminergic and cholinergic neurons of rat nucleus accumbens and caudate-putamen. Furthermore, an enhanced reactivity of nucleus accumbens dopaminergic nerve terminals and dopamine-sensitive cholinergic neurons appears to be a common long-term neuroadaptive effect of distinct types of addictive drugs. However, since repeated ethanol exposure did not cause a long-term increase in the locomotor effect of amphetamine, these neuroadaptations may not always be sufficient to cause long-lasting behavioural (cross-)sensitization.

The aim of this study was to test the effect of a movable backrest on vibration transmission through the trunk during driving and on the physiological consequences thereof. Eleven healthy male subjects drove for about 1 h on normal roads with a movable and with a fixed backrest while surface electromyography (EMG) was measured at the level of the fifth lumbar vertebra (L5) and vertical accelerations were measured at the seat, backrest and at the spine at the levels of the second sacral vertebra (S2) and seventh cervical vertebra (C7). The movable backrest significantly reduced accelerations at C7 by up to 11.9% at the 5 Hz frequency band. The movable backrest also significantly reduced the coherence and transmission between S2 and C7 accelerations, but not the differential motion between these sensors. EMG at both sides of L5 was on average 28% lower when using the movable backrest. Spinal shrinkage was unaffected by backrest type. It is concluded that a movable backrest reduces the transmission of vibration through the trunk and that it reduces low back EMG. Car driving is associated with the risk of developing low back pain and this may be related to exposure to whole body vibration. This study found an effect of a simple ergonomics measure on the transmission of vibration through the trunk as well as on back muscle activation.

Brain activity during resting wakefulness is characterized by slow (<0.1Hz) fluctuations of blood oxygenation level-dependent (BOLD) functional magnetic resonance imaging (fMRI) signals that are topographically organized in discrete functional connectivity networks (resting-state networks, RSNs). The present study aimed at revealing possible network-specific alcohol-induced changes in resting-state fMRI (RS-fMRI) signals. RS-fMRI was carried out on eight healthy subjects in four consecutive 6-min sessions, one before and three after a 0.7 g/kg dose of ethyl alcohol. Control experiments were carried out in different days without alcohol administration. Independent component analysis (ICA) was performed on all experimental and control scans to extract individual and group-level RSN maps in a dynamic network analysis. Alcohol administration significantly increased the overall strength of the visual network ICA component, reaching the peak at 90 min. Within the visual network, the alcohol-induced increase was more pronounced in the primary regions of the occipital cortex and less pronounced in the secondary regions of the occipito-temporal cortex. Other major RSN components, such as the default-mode, the fronto-parietal, the sensori-motor, the self-referential and the auditory components, did not exhibit alcohol-induced changes during the same time window. Alcohol-induced effects on the resting-state functional connectivity of the visual network observed in the present study demonstrate that the visual system is a selective and primary target of acute alcohol administration. The strong enhancement of spontaneous BOLD fluctuations in the primary visual cortex in an acute alcoholic state may impair the normal activation response to visual stimuli and affect visual perception.